Annexin A1 peptide and endothelial cell-conditioned medium modulate cervical tumorigenesis

• Autor(a) principal: Cardin, Laila Toniol [UNESP]
• Data de Publicação: 2019
• Outros Autores: Prates, Janesly [UNESP], da Cunha, Bianca Rodrigues, Tajara, Eloiza Helena, Oliani, Sonia Maria [UNESP], Rodrigues-Lisoni, Flávia Cristina [UNESP]
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UNESP
• Texto Completo: http://dx.doi.org/10.1002/2211-5463.12603; http://hdl.handle.net/11449/189701
• topic: ANXA1; carcinogenesis; cervical cancer; inflammation; peptide treatment

Cervical cancer is one of the leading causes of cancer death in women worldwide, and its tumorigenesis can be influenced by the microenvironment. The anti-inflammatory protein annexin A1 (ANXA1) has been reported to be associated with cancer progression and metastasis, suggesting that it plays a role in regulating tumour cell proliferation. Here, we examined the effect of the N-terminal peptide Ac2-26 of ANXA1 on the HaCaT cell line (normal) and HeLa cell line (cervical cancer) co-cultured with endothelium cell-conditioned medium (HMC). Treatment with Ac2-26 decreased proliferation and increased motility of cervical cancer cells, but did not affect cellular morphology or viability. Combined HMC stimulus and Ac2-26 treatment resulted in an increase in apoptotic HeLa cells, upregulated expression of MMP2, and downregulated expression of COX2, EP3 and EP4. In conclusion, Ac2-26 treatment may modulate cellular and molecular mechanisms underlying cervical carcinogenesis.